Background: Infection with high-risk (HR) human papillomavirus (HPV) is associated with penile cancer in men, cervical cancer in women, and anal cancer and certain types of head and neck cancers in both sexes. Few studies have assessed the prevalence and type distribution of HPV among men in sub-Saharan Africa, where the rates of HIV and penile and cervical cancer are high.
Material and Methods: We used data from a cross-sectional study among 1813 men in Tanzania. Penile samples were tested using Hybrid Capture 2, and genotyping was done by the INNO-LiPA HPV Genotyping Extra test. Blood samples were tested for HIV. The overall and type-specific prevalence and 95% confidence interval of HPV was estimated in relation to age and HIV status.
Results: The overall prevalence of HPV was 20.5% (95% confidence interval, 18.7–22.4), the most prevalent HR HPV types being HPV52, HPV51, HPV16, HPV18, HPV35, and HPV66. The HR HPV prevalence was significantly higher in HIV-positive men (25.7%) than in HIV-negative men (15.8%; P = 0.0027). The prevalence of HPV16, HPV18 and multiple HR HPVs tended to be higher among HIV-positive men (statistically nonsignificant), whereas no differences were observed for the other HPV types.
Conclusions: We found a high prevalence of HPV types 52, 51, 16, 18, 35, and 66. This information is of relevance in the understanding of HPV type distributions across populations. Although the prevalence of HPV16 and HPV18 was slightly higher among HIV-positive men, our results indicate that HIV status does not strongly influence the distribution of HPV types. Therefore, the currently available HPV vaccines could prevent HPV infection independently of HIV status.
The overall prevalence of human papillomavirus (HPV) was 20.5%, with the most prevalent high-risk HPV types being HPV52, HPV51, HPV16, HPV18, and HPV35. There was a tendency toward a higher prevalence of HPV16 and HPV18 among HIV-positive men.
From the *Virus, Lifestyle and Genes, Danish Cancer Society Research Center, Copenhagen, Denmark; †Department of Experimental Virology, Universitaetsklinikum, Tuebingen, Germany; ‡Division of Cancer Prevention, Ocean Road Cancer Institute, Dar es Salaam, United Republic of Tanzania; §Department of Obstetrics and Gynecology, Odense University Hospital, Odense, Denmark; and ¶Gynecologic Clinic, Rigs hospitalet, University of Copenhagen, Copenhagen, Denmark
Supported by Merck (ClinicalTrials.gov ID NCT00932009). The study sponsors had no role in study design, data analysis, data interpretation, writing of the report, or the decision to submit the manuscript for publication.
S.K.K. received lecture fees, advisory board fees, and research grants from Merck and Sanofi Pasteur MSD through her institution. C.M. received lecture fees and travel granted from Merck and Sanofi Pasteur MSD. T.I. received speaker honoraria from Gen-Probe GmbH, Hologic GmbH, and Roche Diagnostics GmbH. For the remaining authors, no conflicts of interest were declared.
Correspondence: Susanne Krüger Kjaer, MD, DMSC, Virus, Lifestyle and Genes, Danish Cancer Society Research Center, Strandboulevarden 49, DK-2100 Copenhagen Ø, Denmark. E-mail: email@example.com.
Received for publication November 13, 2012, and accepted February 28, 2013.